We wish to gain further insight into the molecular events leading to ionizing radiation-induced cell death, and the molecular mechanism of the oxygen effect; more specifically the roles of DNA single- and double-strand breaks and base damage, and their enzymic repair in these processes. We wish to elucidate the biochemical mechanisms and genetic control of the multiple pathways of the repair of radiation-induced damage in bacterial cells, to study the interaction and/or overlap of these different repair pathways, their possible induction by radiation, their selective inhibition by drugs, and to determine which pathways of DNA repair are error free and which are error prone (i.e., mutagenic). The major material for these studies will be the new radiation-sensitive mutants of E. coli K-12 that we have isolated and will continue to isolate in this laboratory, using the new technique of transposon mutagenesis.